Microglial inflammation and phagocytosis in Alzheimer's disease: Potential therapeutic targets

被引：95

作者：

Nizami, Sohaib ^{[1
]}

Hall-Roberts, Hazel ^{[1
,2
]}

Warrier, Sharat ^{[1
,2
]}

Cowley, Sally A. ^{[2
]}

Di Daniel, Elena ^{[1
]}

机构：

[1] Univ Oxford, Alzheimers Res UK Oxford Drug Discovery Inst, Nuffield Dept Med, Res Bldg,Old Rd Campus,Roosevelt Dr, Oxford OX3 7FZ, England

[2] Univ Oxford, Sir William Dunn Sch Pathol, James Martin Stem Cell Facil, Oxford, England

来源：

BRITISH JOURNAL OF PHARMACOLOGY | 2019年 / 176卷 / 18期

关键词：

AMYLOID-BETA; PHARMACOLOGY; 2017/18; CONCISE GUIDE; MOUSE MODEL; NLRP3; INFLAMMASOME; TREM2; DEFICIENCY; TAU PATHOLOGY; COGNITIVE IMPAIRMENT; CORTICAL-NEURONS; PLAQUE-FORMATION;

D O I：

10.1111/bph.14618

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

One of the largest unmet medical needs is a disease-modifying treatment for Alzheimer's disease (AD). Recently, the role of microglia in disease, particularly AD, has gained great interest, following the identification of several disease risk-associated genes that are highly expressed in microglia. Microglia play a critical homeostatic role in the brain, with neuroinflammatory and phagocytic mechanisms being of particular importance. Here, we review the role of NLRP3, the complement system, and the triggering receptor expressed in myeloid cells 2 (TREM2) in modulating microglial functions. We have reviewed the targets, their molecular pathways and the therapeutic interventions aimed at modulating these targets, in the hope of discovering a novel therapeutic approach for the treatment of AD. Linked Articles This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit

引用

页码：3515 / 3532

页数：18

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